Human Ir genes

A number of studies have demonstrated HLA associations with the immune response to different antigens. While it is more difficult to formally demonstrate Ir genes in humans, it is clear that the human MHC gene products function in an analogous manner to the mouse. One example where Ir gene effects in humans most likely play a role is the association of HLA alleles with autoimmune diseases such as ankylosing spondylitis associated with HLA-B27. and rheumatoid arthritis and juvenile onset diabetes associated with HLA-DR4. The H.I.A association is with susceptibility, not resistance, suggesting that the associated HLA antigens may be Ir genes controlling the response to some unknown antigen, either foreign, or self.

Perhaps the most striking and relevant example of Ir gene effects in humans is the demonstration by Hill and colleagues that the HLA-B*530I allele controls the binding of a particular peptide from the liver stage-specific antigen of the malarial parasite, Plasmodium falciparum, thus making B*53()l an immune response gene for this peptide antigen. Most importantly, this peptide represents a critical cytotoxic T lymphocyte epitope and the B'"53()l allele (which is present at greatly increased frequencies in West African populations) confers a high degree of resistance to malaria. Thus, immune response genes in the form of MHC polymorphisms can indeed play a pivotal role in the response to complex antigens such as the malarial parasite, and appear to be capable of evolving due to the influence of natural selection by the pathogen.

See also: Antigen presentation via MHC class I molecules; Antigen presentation via MHC class II molecules; Clonal deletion; Congenic mice; H2 class I; H2 class II; HLA class I; HLA class II; Inbred strains; MHC disease associations; MHC, functions of; MHC restriction; Thymus; T lymphocyte differentiation.

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